Search Result

Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	acute myeloid leukemia
ICD-0-3	NA
Methods	qPCR, Western blot, Luciferase reporter assay, RIP, etc.
Sample	AML cell lines (HL60, KG-1, THP-1, NB4, MOLM-14)
Expression Pattern	up-regulated
Function Description	the low expression level of LINC00319 in whole blood of healthy individuals was obtained from UCSC, and its upregulation was detected in AML patients as well as AML cell lines. Besides, the prognostic significance of LINC00319 was revealed in AML patients. Functionally, the loss-of-function assays revealed that LINC00319 silence restrained proliferation but stimulated apoptosis in AML cells. Furthermore, LINC00319 expression was demonstrated proportional to MYC level in AML samples and transcriptionally regulated by MYC. Mechanistically, we identified FUS as a shared RNA binding protein (RBP) interacting with both LINC00319 and SIRT6. And LINC00319 regulated SIRT6 expression at posttranscriptional level through FUS-dependent pathway. Last but not least, SIRT6 overexpression rescued the suppressive effect of LINC00319 knockdown on AML cells growth.
Pubmed ID	30587342
Year	2019
Title	MYC upregulated LINC00319 promotes human acute myeloid leukemia (AML) cells growth through stabilizing SIRT6.

External Links